Alzheimer's disease (AD) is a common cause of dementia characterized by senile plaques containing β-amyloid peptide (Aβ) and neurofibrillary tangles (NFTs) containing hyperphosphorylated τ-protein. Aβ and phospho-τ may be neurotoxic, leading to progressive neuronal degeneration and death. Despite progress in understanding molecular mechanisms in AD, effective treatment remains elusive. One potential approach to treating AD involves using endogenous neuronal precursors to replace lost or damaged cells. The rostral subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG) can generate neurons into adulthood. Neuronal stem cells in the SVZ give rise to committed progenitor cells that migrate into the olfactory bulb (OB) and differentiate into local interneurons. Progenitors in the SGZ migrate into the granular cell layer and differentiate into neurons. However, the migration of newborn neurons is not restricted to these sites. Endogenous neuronal precursors can proliferate in response to cerebral ischemia and migrate into ischemic regions of striatum and cerebral cortex, and into the CA1 region of hippocampus, where they may integrate into existing brain circuitry and contribute to repair. The proliferation of neuronal stem or progenitor cells in the adult brain is also affected by growth factors, including epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), brain-derived neurotrophic factor (BDNF), stem cell factor (SCF), heparin-binding EGF (HB-EGF), and vascular endothelial growth factor (VEGF). Restoring insulin-like growth factor-I (IGF-I) levels enhances neurogenesis in the aged brain, suggesting that neurogenesis might be augmented by growth factors in vivo in neurodegenerative diseases like AD. Aβ disrupts neurogenesis in SVZ and hippocampus in mouse models of AD, but the status of neurogenesis in neurodegenerative disorders in humans is unknown. We examined the expression of neurogenesis marker proteins in hippocampus of brains from AD patients and neurologically normal subjects. In contrast to findings in animal models, the hippocampus of patients with AD showed increased expression of neurogenesis markers and an increased number of cells expressing these markers, which is consistent with enhanced neurogenesis in human AD. This finding suggests that in AD, as in experimental cerebral ischemia, hippocampal neurogenesis is increased, and might therefore serve to replace hippocampal neurons. As a corollary, measures designed to enhance neurogenesis could have therapeutic value in AD. The study found increased expression of immature neuronal marker proteins in the hippocampus of AD brains, with immunohistochemical localization to hippocampal sites of neurogenesis (DG) and of AD pathology (CA1). The up-regulated proteins included DCX, PSA-Alzheimer's disease (AD) is a common cause of dementia characterized by senile plaques containing β-amyloid peptide (Aβ) and neurofibrillary tangles (NFTs) containing hyperphosphorylated τ-protein. Aβ and phospho-τ may be neurotoxic, leading to progressive neuronal degeneration and death. Despite progress in understanding molecular mechanisms in AD, effective treatment remains elusive. One potential approach to treating AD involves using endogenous neuronal precursors to replace lost or damaged cells. The rostral subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG) can generate neurons into adulthood. Neuronal stem cells in the SVZ give rise to committed progenitor cells that migrate into the olfactory bulb (OB) and differentiate into local interneurons. Progenitors in the SGZ migrate into the granular cell layer and differentiate into neurons. However, the migration of newborn neurons is not restricted to these sites. Endogenous neuronal precursors can proliferate in response to cerebral ischemia and migrate into ischemic regions of striatum and cerebral cortex, and into the CA1 region of hippocampus, where they may integrate into existing brain circuitry and contribute to repair. The proliferation of neuronal stem or progenitor cells in the adult brain is also affected by growth factors, including epidermal growth factor (EGF), fibroblast growth factor-2 (FGF-2), brain-derived neurotrophic factor (BDNF), stem cell factor (SCF), heparin-binding EGF (HB-EGF), and vascular endothelial growth factor (VEGF). Restoring insulin-like growth factor-I (IGF-I) levels enhances neurogenesis in the aged brain, suggesting that neurogenesis might be augmented by growth factors in vivo in neurodegenerative diseases like AD. Aβ disrupts neurogenesis in SVZ and hippocampus in mouse models of AD, but the status of neurogenesis in neurodegenerative disorders in humans is unknown. We examined the expression of neurogenesis marker proteins in hippocampus of brains from AD patients and neurologically normal subjects. In contrast to findings in animal models, the hippocampus of patients with AD showed increased expression of neurogenesis markers and an increased number of cells expressing these markers, which is consistent with enhanced neurogenesis in human AD. This finding suggests that in AD, as in experimental cerebral ischemia, hippocampal neurogenesis is increased, and might therefore serve to replace hippocampal neurons. As a corollary, measures designed to enhance neurogenesis could have therapeutic value in AD. The study found increased expression of immature neuronal marker proteins in the hippocampus of AD brains, with immunohistochemical localization to hippocampal sites of neurogenesis (DG) and of AD pathology (CA1). The up-regulated proteins included DCX, PSA-